ERK plays the baddie (again)

It has been known for many years that elevated signaling by the ERK1/2 pathway is frequently associated with the growth and survival of many tumor cell types under a variety of normal and stressful conditions, including the response of cells to other cancer interventional therapeutic strategies e.g., references 1–4. There is, however, a modest significant literature showing that enhanced ERK1/2 signaling can also cause tumor cell death e.g., references 5–8. The role of ERK1/2 signaling is clearly complex, for example as shown by the Koumenis group where inhibition of radiation-induced ERK1/2 signaling caused radiosensitization, whereas inhibition of curcumin-hyper-stimulated ERK1/2 signaling reduced radiosensitivity.(7) Presumably this Janus-faced behavior of the ERK1/2 pathway in terms of cell survival regulation will depend upon the tumor cell type, the intensity of ERK1/2 stimulation, and the molecular intervention/drug being used.